Gastric acid secretion !
- Mechanism
- Exam priority: high
Parietal cells pump acid into the stomach with the H⁺/K⁺ pump; the vagus, gastrin and histamine turn it on, and somatostatin turns it off.
Updated 2026-11-01
Also called: Parietal cell, Proton pump
See it in 3D: Stomach · Vagus nerve · Vagal trunks
What it is
The parietal cell of the gastric body and fundus glands secretes hydrochloric acid and intrinsic factor. The last step is the apical H⁺/K⁺-ATPase, which swaps H⁺ for K⁺ using ATP. Three stimuli converge on it (acetylcholine, gastrin and histamine) and one main brake (somatostatin) shuts it down as pH falls.
How it works, step by step
- Inside the parietal cell, carbonic anhydrase turns CO₂ and water into H⁺ and HCO₃⁻.
- HCO₃⁻ leaves across the basolateral membrane in exchange for Cl⁻ (Cl⁻/HCO₃⁻ exchanger): chloride enters and the alkaline tide begins.
- On stimulation, tubulovesicles carrying the H⁺/K⁺-ATPase fuse with the canaliculi and multiply the secreting surface.
- The pump moves H⁺ into the lumen and K⁺ into the cell; K⁺ leaks back out through apical channels and Cl⁻ exits through chloride channels: the result is HCl.
- Acetylcholine and gastrin raise intracellular Ca²⁺; histamine raises cAMP; both routes activate protein kinases that keep the pump in the membrane.
- When antral pH falls below ≈3, D cells release somatostatin, which inhibits G cells, ECL cells and the parietal cell itself (negative feedback).
- In the duodenum, acid, fat and hyperosmolality release secretin and other signals that also reduce gastric secretion.
Reference values (adult)
| Parameter | Value | Note |
|---|---|---|
| Gastric juice pH | ≈1–3 | when stimulated |
| Gastric secretion volume | ≈1.5–2.5 L/day | |
| H⁺ concentration in pure juice | ≈150 mEq/L | ≈3 million times that of plasma |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Regulation
- +Vagus (acetylcholine, M3) and GRP: Stimulates the parietal cell directly and releases gastrin; dominates the cephalic phase
- +Gastrin: Releases histamine from ECL cells and stimulates the parietal cell; triggered by peptides and distension
- +Histamine (H2): Raises cAMP and potentiates the other two stimuli
- −Somatostatin (D cells): Inhibits gastrin, histamine and acid as gastric pH falls
- −Prostaglandins (PGE₂): Lower acid and raise protective mucus and bicarbonate
- −Secretin, GIP and the enterogastric reflex: The duodenum brakes the stomach when acid or fat arrives
Clinical notes
- NSAIDs block prostaglandin synthesis: less mucus and bicarbonate, more effective acid → gastritis and ulcer.
- Antral H. pylori lowers somatostatin → more gastrin and acid → duodenal ulcer; infection of the whole gastric body causes atrophy and low acid.
- Persistent vomiting loses HCl → hypochloremic, hypokalemic metabolic alkalosis.
- Long-term acid suppression: less absorption of non-heme iron and of food-bound vitamin B12.
Test yourself
Think of the answer, then tap the question to see it.
Why does a proton pump inhibitor suppress acid more effectively than an H2 blocker?
It blocks the H⁺/K⁺-ATPase, the final common step of all three stimuli. An H2 blocker removes only the histamine route, so acetylcholine and gastrin still drive some secretion.
What is the alkaline tide and why does it happen after meals?
A rise in bicarbonate in gastric venous blood: for every H⁺ the parietal cell secretes into the lumen, one HCO₃⁻ leaves into the blood in exchange for Cl⁻.
How does antral H. pylori infection lead to more acid and a duodenal ulcer?
The bacterium damages antral D cells and lowers somatostatin; without that brake gastrin rises, acid secretion increases and the excess acid reaches the duodenum.
Why does autoimmune atrophic gastritis cause megaloblastic anemia as well as achlorhydria?
Antibodies destroy parietal cells, which make both acid and intrinsic factor. Without intrinsic factor, vitamin B12 cannot be absorbed in the terminal ileum.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Gastrointestinal hormones
- Vomiting and its control
- Absorption of iron, calcium and vitamin B12
- Protein digestion and absorption
- Metabolic alkalosis and its compensation
Related conditions
- Peptic ulcer disease
- Helicobacter pylori gastritis
- Gastro-oesophageal reflux disease (GERD)
- Pernicious anaemia
- Upper gastrointestinal bleeding
- Metabolic alkalosis
In Biochemistry
In Pharmacology
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 23.4 The Stomach (OpenStax (Rice University), 2022); Peptic Ulcer Disease (StatPearls (NCBI Bookshelf), 2024); Gastroesophageal Reflux Disease (GERD) (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 65). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.